Cardiac oxidative stress and remodeling following infarction: role of NADPH oxidase

Zhao, Wenyuan; Zhao, Dan; Yan, Ran; Sun, Yao

doi:10.1016/j.carpath.2007.12.013

Cited by 39 publications

(41 citation statements)

References 41 publications

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“…Several pieces of evidence have implicated the TGF-␤ system as a major etiological agent in the pathogenesis of cardiac fibrosis, including type III collagen overexpression and LV remodeling in AMI. 8,35,36 Because latent TGF-␤ can be activated in vitro on oxidative stress generation, 39 anti-oxidative properties of PEDF could contribute directly to its antifibrotic effects in our AMI model as well.…”

Section: Discussionmentioning

confidence: 98%

Administration of Pigment Epithelium-Derived Factor Inhibits Left Ventricular Remodeling and Improves Cardiac Function in Rats with Acute Myocardial Infarction

Ueda

Yamagishi

Matsui

et al. 2011

The American Journal of Pathology

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Oxidative stress and inflammation are involved in cardiac remodeling after acute myocardial infarction (AMI). We have found that pigment epithelium-derived factor (PEDF) inhibits vascular inflammation through its anti-oxidative properties. However, effects of PEDF on cardiac remodeling after AMI remain unknown. We investigated whether PEDF could inhibit left ventricular remodeling and improve cardiac function in rats with AMI. AMI was induced in 8-weekold Sprague-Dawley rats by ligation of the left ascending coronary artery. Rats were treated intravenously with vehicle or 10 g PEDF/100 g b.wt. every day for up to 2 weeks after AMI. Each rat was followed until 16 weeks of age. PEDF levels in infarcted areas and serum were significantly decreased at 1 week after AMI and remained low during the observational periods. PEDF administration inhibited apoptotic cell death and oxidative stress generation around the infarcted areas at 2 and 8 weeks after AMI. Further, PEDF injection suppressed cardiac fibrosis by reducing transforming growth factor-␤ and type III collagen expression, improved left ventricular ejection fraction, ameliorated diastolic dysfunction, and inhibited the increase in left ventricular mass index at 8 weeks after AMI. The present study demonstrated that PEDF could inhibit tissue remodeling and improve cardiac function in AMI rats. Substitution of PEDF may be a novel therapeutic strategy for cardiac remodeling after AMI.

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Section: Discussionmentioning

confidence: 98%

Administration of Pigment Epithelium-Derived Factor Inhibits Left Ventricular Remodeling and Improves Cardiac Function in Rats with Acute Myocardial Infarction

Ueda

Yamagishi

Matsui

et al. 2011

The American Journal of Pathology

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“…NADPH oxidase is the main source of myocardial ROS. Studies show that the accumulation of fibroblasts and deposition of collagen were reduced in myocardial-infarction mice and that the mice had lower blood pressures after Nox2 knockout, while the excessive proliferation of blood vessels induced by Ang II was prevented [31]. Nox4 plays an important role in myocardial hypertrophy, fibrosis and myocardial apoptosis in pressure-overloaded mice and is important in the process of ageing of the heart [32,33,34].…”

Section: Discussionmentioning

confidence: 99%

Erythropoietin Decreases the Occurrence of Myocardial Fibrosis by Inhibiting the NADPH-ERK-NF-κB Pathway

Wang¹,

Yang²,

Wang³

et al. 2015

Cardiology

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Objectives: The aim of this study was to investigate the protective role of erythropoietin (EPO) against myocardial fibrosis (MF). Methods: Pressure-overloaded rats were established by abdominal aortic constriction, the rats were randomly divided in a double-blind manner into 3 groups (n = 12 for each group): sham-operated rats (sham), operated rats receiving physiological saline (vehicle) and operated rats receiving 4,000 U/kg rhEPO (EPO group). The vehicle and drugs were administered to rats by intraperitoneal injection. In addition, cultured adult rat cardiac fibroblasts (CFs) were utilized to investigate the role of EPO in CF proliferation and collagen secretion. Results: After 4 weeks, besides an increase in blood pressure, myocardial hypertrophy, collagen deposition in the myocardium and decreased cardiac function were observed in the pressure-overloaded rats. The expression of NADPH oxidase (Nox2 and Nox4) and inflammatory cytokines (CD45, F4/80 and MCP-1) was also significantly increased. All these alterations were prevented by EPO. TGF-ß promoted CF proliferation, collagen secretion, ROS production and Nox2/Nox4 expression, which was inhibited by EPO. In addition, the TGF-ß-induced increase of ERK1/2 phosphorylation and NF-κB expression were attenuated by EPO. Conclusion: EPO inhibited rat MF induced by pressure overload and improved myocardial function by decreasing CF proliferation and differentiation via inhibition of the NADPH-ERK-NF-κB pathway.

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“…Furthermore, Nox2 seem to play a crucial role in preconditioning during the early ischemic phase. Recent studies have demonstrated that gp91phox expression was significantly increased in the infarcted myocardium of mice, particularly in the early stage of MI (20). Monocytederived macrophages were found to be the major inflammatory cells in the infarcted myocardium, mainly characterized by increased expression of gp91phox (20).…”

Section: Ros In Myocardial Infarction and Ischemia-reperfusion Injurymentioning

confidence: 99%

“…Monocytederived macrophages were found to be the major inflammatory cells in the infarcted myocardium, mainly characterized by increased expression of gp91phox (20). The expression pattern of macrophages gp91phox is similar to the expression of NADPH in overall myocardial tissue, with a declining phase 2 weeks after MI, thus indicating macrophages as a dominant source of ROS in infracted myocardium (20). Additional data also showed that lack of p47phox subunit, could improve cardiac function and survival in p47phox knockout mice, after experimentally induced MI (21).…”

Section: Ros In Myocardial Infarction and Ischemia-reperfusion Injurymentioning

confidence: 99%

“…Recent studies have demonstrated that gp91phox expression was significantly increased in the infarcted myocardium of mice, particularly in the early stage of MI (20). Monocytederived macrophages were found to be the major inflammatory cells in the infarcted myocardium, mainly characterized by increased expression of gp91phox (20). The expression pattern of macrophages gp91phox is similar to the expression of NADPH in overall myocardial tissue, with a declining phase 2 weeks after MI, thus indicating macrophages as a dominant source of ROS in infracted myocardium (20).…”

Section: Ros In Myocardial Infarction and Ischemia-reperfusion Injurymentioning

confidence: 99%

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The role of reactive oxygen species in the pathophysiology of cardiovascular diseases and the clinical significance of myocardial redox

et al. 2017

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Acute and chronic excessive intracellular increase of reactive oxygen species (ROS) is involved in the development and progression of cardiovascular diseases. ROS are by-products of various oxidative physiological and biochemical processes. Sources of ROS are mitochondrial respiration, NADH/NADPH oxidase, xanthine oxidoreductase or the uncoupling of nitric oxide synthase (NOS) in vascular cells. ROS mediate various signaling pathways that underlie cardiovascular pathophysiology. The delicate equilibrium between free-radical generation and antioxidant defense is altered in favor of the former, thus leading to redox imbalance, oxidative stress, and increased cellular injury. An understanding of the pathophysiological mechanisms mediated by oxidative stress is crucial to the prevention and treatment of cardiovascular diseases.

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Cardiac oxidative stress and remodeling following infarction: role of NADPH oxidase

Cited by 39 publications

References 41 publications

Administration of Pigment Epithelium-Derived Factor Inhibits Left Ventricular Remodeling and Improves Cardiac Function in Rats with Acute Myocardial Infarction

Administration of Pigment Epithelium-Derived Factor Inhibits Left Ventricular Remodeling and Improves Cardiac Function in Rats with Acute Myocardial Infarction

Erythropoietin Decreases the Occurrence of Myocardial Fibrosis by Inhibiting the NADPH-ERK-NF-κB Pathway

The role of reactive oxygen species in the pathophysiology of cardiovascular diseases and the clinical significance of myocardial redox

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